1. Field of the Invention
This disclosure is related to the field of systems and methods for optical lens reformation. Specifically, this disclosure is related to the field of systems and methods for using electromagnetic energy to make physical and biochemical alterations to the ocular lens of a mammalian eye for the correction of visual impairments.
2. Description of Related Art
Cataracts are areas of opacification of the ocular lens of sufficient size to interfere with vision. They have been extensively studied because of their high prevalence in geriatric populations. Cataracts in the aged (senile cataracts) are the most common type, and are often thought to be due to an acceleration of the scattering of light as it passes through the lens of an eye. Cataracts occur to varying extents in all humans over the age of 50, but generally do not cause significant visual dysfunction until the ages of 60-80 years. In some instances, however, cataracts can occur much earlier as a result of risk factors including congenital disease, trauma, and family history.
FIG. 2 and FIG. 3 are presented as an aid to understanding the visual impairments related to the ocular lens, such as the formation of cataracts. The ocular lens is a multi-structural system as illustrated in FIGS. 2 and 3. As will be understood by those of ordinary skill in the art, the macroscopic lens structure includes a cortex just inside the capsule, which is the outer membrane that envelops the other interior structures of the lens. The nuclei are formed from successive additions of the cortex (13) to the nuclear regions, which are subdivided into a deep fetal nucleus (22) which develops in the womb, an infantile nucleus (24), a juvenile nucleus (26), and the adult nucleus (28). On the microscopic level, the structure of the nuclei is layered, resembling the structure of an onion with the oldest layers and cells towards the center (and as depicted in FIG. 2). Rather than being spherical, the lens is a bioconvex shape as shown in FIG. 2. The cortex and the different nuclei have specific structures that are consistent through different ages for specific cell sizes, compactions and clarity. The lens epithelium (23) forms at the lens equatorial region (21) generating ribbon-like cells or fibrils that grow anteriorly and posteriorly around the ocular lens. The unique formation of the crystalline lens is the biconvex shape depicted in FIG. 3 where the ends of the cells align to form a suture in the central and paracentral areas (29) both anteriorly and posteriorly. Transparency is maintained by the regular architecture of the fibrils. As long as the regular architecture is maintained, light passes unobstructed through the lens. The older tissue in both the cortex and nucleus has reduced cellular function, having lost their cell nuclei and other organelles several months after cell formation. The aqueous (17), the liquid in the anterior chamber between the lens and cornea which also contains ionic components and solutes, flows through the lens capsule (14) and sutures. From there, the ions and/or fluids travel into more remote areas of the lens and provide the nutrients needed for minimal cellular life functions, including the removal of toxic and oxidative byproducts.
The microstructure of the fibrils contains interconnections between the ribbon-like fibrils, called balls and sockets, and interdigitations and imprints, which to some extent inhibit the relative motion of fibrils with respect to one another. Still, the fibrils are relatively free to move in relation to each other in the young, flexible crystalline lens. As the eye ages, there are age related changes to these structures that include the development of intracellular bonding, mostly disulfide bonding, the compaction of tissue, the breakdown of some of the original attachments, and the yellowing or darkening of older lens areas.
Changes in the size and shape of the macroscopic lens components throughout life include both the increased curvature and general enlargement of the biconvex lens with age. The thickness of the posterior portion increases more than the anterior portion. Additionally, thickness increases are proportionately greater in the periphery.
The above-mentioned intracellular bonding that occurs with age generally immobilizes the oldest and deepest lens tissue. However, intracellular disulfide bonds are weaker chemical bonds, and are subject to modification and breakage with minute laser pulses. The disulfide bonds are largely formed by the effects of ambient ultraviolet (UV) light from external exposure and from the continual, unrelenting reduction in lens movement with age (presbyopia). The lens absorbs ions and nutrients from the aqueous, a process enhanced by lens accommodation; e.g., the undulating movement of the younger crystalline lens. The aqueous normally contains the amino acid building blocks of antioxidants that aid in preventing disulfide bond formation that further inhibits lens movement and, accordingly, loss of ion and nutrient absorption can lead to presbyopia, cataracts, glaucoma and other related eye conditions.
In summary, presbyopia, light scattering and cataractogenesis generally result from intrafibril attachment. On the cellular level, all cataracts begin with oxidative changes of the crystalline tissue. The changes in the lens tissue that lead to light scattering occur when individual fibers combine to form large, light-disrupting macromolecular complexes.
Generally, the two different processes that lead to presbyopia, light scattering and cataracts, occur simultaneously and continuously, but at different rates. The possible connection between the two processes was clarified by Cook and Koretz, et al. (Invest. Ophthal. Vis. Science (1994)), the entirety of which is specifically incorporated herein by reference to the extent not inconsistent with the disclosures of this patent. Koretz, et al. studied extensively the presence of zones of light scatter. They not only confirmed that older lenses had more light scatter, but also they reported an acceleration in the rate of formation of light-scattering macromolecular complexes starting in the fourth decade of life. Koretz theorized that reduced lens movement due to decreased accommodation reduces the active transport leaving only diffusion and exacerbates the process leading to light scattering.
In order to understand the impact of the methods and systems disclosed herein, it is important to clarify the lens structure with its different segments or shells that form during the ageing process. Thus, as further foundation for this discussion, the anatomical structures of the eye are further shown in FIG. 1, a cross sectional view of the eye. The sclera (31) is the white tissue that surrounds the lens except at the cornea. The cornea (1) is the transparent tissue that comprises the exterior surface of the eye through which light first enters the eye. The iris (2) is a colored, contractible membrane that controls the amount of light entering the eye by changing the size of the circular aperture at its center (the pupil). The ocular or crystalline lens (3), a more detailed picture of which is shown in FIG. 2, is located just posterior to the iris. Generally the ocular lens changes shape through the action of the ciliary muscle (8) to allow for focusing of a visual image. A neural feedback mechanism from the brain allows the ciliary muscle (8), acting through the attachment of the zonules (11), to change the shape of the ocular lens. Generally, sight occurs when light enters the eye through the cornea (1) and pupil, then proceeds past the ocular lens (3) through the vitreous (10) along the visual axis (4), strikes the retina (5) at the back of the eye, forming an image at the macula (6) that is transferred by the optic nerve (7) to the brain. The space between the cornea and the retina is filled with a liquid called the aqueous in the anterior chamber (9) and the vitreous (10), a gel-like, clear substance posterior to the lens.
Generally, the optical characteristics of the eye are determined by the clear tissue and fluids between the cornea (1) and the retina (5). The cornea (1) is a stiff, transparent tissue with a stable curvature confining and protecting the eye contents. The cornea (1) has passive optical characteristics compared with the crystalline lens (3) where the flexible optics actively change refractive error. This is the only structure in the eye that contributes to a change in focusing. In a posterior direction into the eye, there is the fluid called the aqueous (9), then the crystalline lens (3) and the vitreous (10). The fluids of the eye, the aqueous and the vitreous have very little impact upon refraction because they are so close to the refractive index (i.e., the optical density) of adjacent tissues.
Presbyopia is the loss of focusing that occurs when the crystalline lens loses its flexural characteristics sufficient to require auxiliary focusing—i.e., reading glasses or bifocals. Generally, people begin to lose flexibility in their crystalline lenses in their 40s and by age 50 the lens has negligible flexure. There is regularity about presbyopia development that is innate and varies little with disease except in diabetes where presbyopia can come several years earlier. Virtually all humans eventually lose all lens movement except for the outermost areas of the tissue.
The flexure of the lens (3) is illustrated by the accommodative changes that are present in lenses of different ages. For example, it has been shown that flexure can vary as much as about 12-16 diopters, allowing for about a 6-8 cm focus in a 5-year-old to about 50 centimeters or less for a 50-year-old lens. The ciliary muscle (8) stretches while the lens distends for observing distance, and then relaxes returning the focus at near and the lens returns to its actual shape. In an older lens there is little or no distension of the lens, although researchers have shown the ciliary muscle persists in movement even in older, immovable lenses.
There is an anatomical pattern of the development of the crystalline lens (3) that is a characteristic of age. The decline in accommodation, measured by diopters of accommodation, as well as concomitant clarity changes (e.g., zones of discontinuity or increased light scatter), have a high correlation to age. The net result of these irreversible changes continues unless, as this application proposes, there is a change in the transport of ions/fluids to that area. Such changes in clarity are the age-related changes from light scatter which theoretically might result in a cataract when opacification is too great to continue with useful vision. Cataracts, especially in populations under 70-years-old, are more likely from other types caused by systemic disease or other localized mechanisms.
The physiological explanation of light scatter development is that active oxygen is always present and travels from the aqueous and the vitreous into the lens and through the crystalline fibers. This active oxygen causes covalent chemical bonding between the surfaces of the lens fibers, unless specific antioxidants are present to counter the attachments. Once formed, these attachments not only produce sites of light scatter, but reduce the movement between individual fibers. As noted previously, the most common bonds are referred to as disulfide or covalent chemical bonding, which form at a relatively low energy level of chemical bonding. This reduction in movement and bonding produces cascading modification of localized tissue, including compaction and reduction in ionic/fluid transport.
In the ophthalmic literature going back to the early 1900's a paradoxical observation was observed in incidences where foreign bodies such as iron, glass or copper wires enter the eye and sometimes embed in the lens. In most occurrences, the lens becomes cataractous. However, as early as the 1900's, there were reports of embedded objects without cataract development. Some years later, it was shown that these objects did not cause massive infections or inflammations, or affect other ocular tissues, when they were sufficiently small to allow the lens capsule to reseal itself. The significance of this observation was that a foreign body could remain for periods of generally up to 40 years without developing inflammation or a localized or complete cataract. Imbedded foreign bodies demonstrate the inert properties of a crystalline lens without a significant reaction to the outside penetration.